Some class-specific anti-collagens may be specific for three-dimensional epitopes which may result in diminished reactivity with denatured collagen or formalin-fixed, paraffin embedded tissues

Biohazard Information

This product contains sodium azide as preservative. Although the amount of sodium azide is very small appropriate care must be taken when handling this product.

Immunogen

Collagen type III antibody was raised in rabbit using collagen type III from human and bovine placenta as the immunogen.

Preparation and Storage

Store at 4 degree C for short term storage. Aliquot and store at -20 degree C for long term storage. Avoid repeated freeze/thaw cycles.

Other Notes

Small volumes of anti-COL3A1 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

This gene encodes the pro-alpha1 chains of type III collagen, a fibrillar collagen that is found in extensible connective tissues such as skin, lung, uterus, intestine and the vascular system, frequently in association with type I collagen. Mutations in this gene are associated with Ehlers-Danlos syndrome types IV, and with aortic and arterial aneurysms. Two transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008]

UniProt Comments for COL3A1

CO3A1: Collagen type III occurs in most soft connective tissues along with type I collagen. Defects in COL3A1 are a cause of Ehlers-Danlos syndrome type 3 (EDS3); also known as benign hypermobility syndrome. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS3 is a form of Ehlers-Danlos syndrome characterized by marked joint hyperextensibility without skeletal deformity. Defects in COL3A1 are the cause of Ehlers-Danlos syndrome type 4 (EDS4). EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS4 is the most severe form of the disease. It is characterized by the joint and dermal manifestations as in other forms of the syndrome, characteristic facial features (acrogeria) in most patients, and by proneness to spontaneous rupture of bowel and large arteries. The vascular complications may affect all anatomical areas. Defects in COL3A1 are a cause of susceptibility to aortic aneurysm abdominal (AAA). AAA is a common multifactorial disorder characterized by permanent dilation of the abdominal aorta, usually due to degenerative changes in the aortic wall. Histologically, AAA is characterized by signs of chronic inflammation, destructive remodeling of the extracellular matrix, and depletion of vascular smooth muscle cells. Belongs to the fibrillar collagen family. 2 isoforms of the human protein are produced by alternative splicing.

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